Autism Studies and Related Medical Conditions, January 2009 - TACA

contributing factors may contribute to autism spectrum disorders by provoking
innate and adaptive immune reactions to cause and perpetuate effects in
susceptible individuals that result in inflammation, molecular mimicry, kynurenine
pathway changes, increased quinolinic acid and decreased serotonin, oxidative
stress, mitochondrial dysfunction and excitotoxicity that impair the development
of the amygdala and other neural structures and neural networks resulting in a
partial Kluver-Bucy Syndrome and other deficits resulting in autism spectrum
disorders and/or exacerbating autism spectrum disorders from other causes
throughout life. Support for this hypothesis includes multiple cases of mothers
with Lyme disease and children with autism spectrum disorders; fetal
neurological abnormalities associated with tick-borne diseases; similarities
between tick-borne diseases and autism spectrum disorder regarding symptoms,
pathophysiology, immune reactivity, temporal lobe pathology, and brain imaging
data; positive reactivity in several studies with autistic spectrum disorder patients
for Borrelia burgdorferi (22%, 26% and 20-30%) and 58% for mycoplasma;
similar geographic distribution and improvement in autistic symptoms from
antibiotic treatment. It is imperative to research these and all possible causes of
autism spectrum disorders in order to prevent every preventable case and treat
every treatable case until this disease has been eliminated from humanity.
Chauhan, A. and V. Chauhan (2006). "Oxidative stress in autism." Pathophysiology
13(3): 171-81.
Autism is a severe developmental disorder with poorly understood etiology.
Oxidative stress in autism has been studied at the membrane level and also by
measuring products of lipid peroxidation, detoxifying agents (such as
glutathione), and antioxidants involved in the defense system against reactive
oxygen species (ROS). Lipid peroxidation markers are elevated in autism,
indicating that oxidative stress is increased in this disease. Levels of major
antioxidant serum proteins, namely transferrin (iron-binding protein) and
ceruloplasmin (copper-binding protein), are decreased in children with autism.
There is a positive correlation between reduced levels of these proteins and loss
of previously acquired language skills in children with autism. The alterations in
ceruloplasmin and transferrin levels may lead to abnormal iron and copper
metabolism in autism. The membrane phospholipids, the prime target of ROS,
are also altered in autism. The levels of phosphatidylethanolamine (PE) are
decreased, and phosphatidylserine (PS) levels are increased in the erythrocyte
membrane of children with autism as compared to their unaffected siblings.
Several studies have suggested alterations in the activities of antioxidant
enzymes such as superoxide dismutase, glutathione peroxidase, and catalase in
autism. Additionally, altered glutathione levels and homocysteine/methionine
metabolism, increased inflammation, excitotoxicity, as well as mitochondrial and
immune dysfunction have been suggested in autism. Furthermore, environmental
and genetic factors may increase vulnerability to oxidative stress in autism.
Taken together, these studies suggest increased oxidative stress in autism that
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